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Overall, these observations, combined with the results of mass spectrometry and KEAP1 mutant analysis and the fact that TNBCs are characterized by a truly low rate of somatic mutations and CNV of NFE2L2 and genes encoding key components of the NRF2 degradation pathway, are consistent with the hypothesis that forced Cyss uptake by overexpression of SLC7A11 induces KEAP1 inactivation via cysteinylation of sensor residues 226 and 613